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AKAP12 Overexpression Affects Cardiac Function via PDE8

德国的 医学 老年学 哲学 语言学
作者
Hariharan Subramanian,Viacheslav O. Nikolaev
出处
期刊:Circulation Research [Ovid Technologies (Wolters Kluwer)]
卷期号:134 (8): 1023-1025
标识
DOI:10.1161/circresaha.124.324475
摘要

HomeCirculation ResearchVol. 134, No. 8AKAP12 Overexpression Affects Cardiac Function via PDE8 No AccessEditorialRequest AccessFull TextAboutView Full TextView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toNo AccessEditorialRequest AccessFull TextAKAP12 Overexpression Affects Cardiac Function via PDE8 Hariharan Subramanian and Viacheslav O. Nikolaev Hariharan SubramanianHariharan Subramanian https://orcid.org/0000-0001-5409-4856 Institute of Experimental Cardiovascular Research, University Medical Center Hamburg-Eppendorf, Germany (H.S., V.O.N.). German Center for Cardiovascular Research (DZHK), Partner Site Hamburg/Kiel/Lübeck, Germany (H.S., V.O.N.). and Viacheslav O. NikolaevViacheslav O. Nikolaev Correspondence to: Viacheslav O. Nikolaev, PhD, Institute of Experimental Cardiovascular Research, University Medical Center, Hamburg-Eppendorf Martinistr. 52, House W23, D-20246, Hamburg, Germany. Email E-mail Address: [email protected] https://orcid.org/0000-0002-7529-5179 Institute of Experimental Cardiovascular Research, University Medical Center Hamburg-Eppendorf, Germany (H.S., V.O.N.). German Center for Cardiovascular Research (DZHK), Partner Site Hamburg/Kiel/Lübeck, Germany (H.S., V.O.N.). Originally published11 Apr 2024https://doi.org/10.1161/CIRCRESAHA.124.324475Circulation Research. 2024;134:1023–1025This article is a commentary on the followingAKAP12 Upregulation Associates With PDE8A to Accelerate Cardiac DysfunctionFootnotesThe opinions expressed in this article are not necessarily those of the editors or of the American Heart Association.For Sources of Funding and Disclosures, see page 1025.Correspondence to: Viacheslav O. Nikolaev, PhD, Institute of Experimental Cardiovascular Research, University Medical Center, Hamburg-Eppendorf Martinistr. 52, House W23, D-20246, Hamburg, Germany. Email v.nikolaev@uke.deREFERENCES1. Subramanian H, Nikolaev VO. A-kinase anchoring proteins in cardiac myocytes and their roles in regulating calcium cycling.Cells. 2023; 12:436. doi: 10.3390/cells12030436CrossrefMedlineGoogle Scholar2. McConnell BK, Popovic Z, Mal N, Lee K, Bautista J, Forudi F, Schwartzman R, Jin JP, Penn M, Bond M. Disruption of protein kinase A interaction with A-kinase-anchoring proteins in the heart in vivo: effects on cardiac contractility, protein kinase A phosphorylation, and troponin I proteolysis.J Biol Chem. 2009; 284:1583–1592. doi: 10.1074/jbc.M806321200CrossrefMedlineGoogle Scholar3. Fink MA, Zakhary DR, Mackey JA, Desnoyer RW, Apperson-Hansen C, Damron DS, Bond M. AKAP-mediated targeting of protein kinase a regulates contractility in cardiac myocytes.Circ Res. 2001; 88:291–297. doi: 10.1161/01.res.88.3.291LinkGoogle Scholar4. Diviani D, Dodge-Kafka KL, Li J, Kapiloff MS. A-kinase anchoring proteins: scaffolding proteins in the heart.Am J Physiol Heart Circ Physiol. 2011; 301:H1742–H1753. doi: 10.1152/ajpheart.00569.2011CrossrefMedlineGoogle Scholar5. Jones BW, Brunet S, Gilbert ML, Nichols CB, Su T, Westenbroek RE, Scott JD, Catterall WA, McKnight GS. Cardiomyocytes from AKAP7 knockout mice respond normally to adrenergic stimulation.Proc Natl Acad Sci U S A. 2012; 109:17099–17104. doi: 10.1073/pnas.1215219109CrossrefMedlineGoogle Scholar6. Nichols CB, Rossow CF, Navedo MF, Westenbroek RE, Catterall WA, Santana LF, McKnight GS. Sympathetic stimulation of adult cardiomyocytes requires association of AKAP5 with a subpopulation of L-type calcium channels.Circ Res. 2010; 107:747–756. doi: 10.1161/CIRCRESAHA.109.216127LinkGoogle Scholar7. Kritzer MD, Li J, Passariello CL, Gayanilo M, Thakur H, Dayan J, Dodge-Kafka K, Kapiloff MS. The scaffold protein muscle A-kinase anchoring protein beta orchestrates cardiac myocyte hypertrophic signaling required for the development of heart failure.Circ Heart Fail. 2014; 7:663–672. doi: 10.1161/CIRCHEARTFAILURE.114.001266LinkGoogle Scholar8. Ghigo A, Perino A, Mehel H, Zahradnikova A, Morello F, Leroy J, Nikolaev VO, Damilano F, Cimino J, De Luca E, et al. Phosphoinositide 3-kinase gamma protects against catecholamine-induced ventricular arrhythmia through protein kinase A-mediated regulation of distinct phosphodiesterases.Circulation. 2012; 126:2073–2083. doi: 10.1161/CIRCULATIONAHA.112.114074LinkGoogle Scholar9. Guillory AN, Yin X, Wijaya CS, Diaz Diaz AC, Rababa'h A, Singh S, Atrooz F, Sadayappan S, McConnell BK. Enhanced cardiac function in Gravin mutant mice involves alterations in the beta-adrenergic receptor signaling cascade.PLoS One. 2013; 8:e74784. doi: 10.1371/journal.pone.0074784CrossrefMedlineGoogle Scholar10. Hanan Qasim MR, Ying X, Arfaxad R-A, Hala A, Satadru KL, Xander HTW, Bradley KM. Akap12 upregulation reduces intracellular cAMP levels and deteriorates cardiac function.Circ Res. 2024; 132:1006–1022. doi: 10.1161/CIRCRESAHA.123.323655LinkGoogle Scholar11. Willoughby D, Wong W, Schaack J, Scott JD, Cooper DM. An anchored PKA and PDE4 complex regulates subplasmalemmal cAMP dynamics.EMBO J. 2006; 25:2051–2061. doi: 10.1038/sj.emboj.7601113CrossrefMedlineGoogle Scholar12. Grammatika Pavlidou N, Dobrev S, Beneke K, Reinhardt F, Pecha S, Jacquet E, Abu-Taha IH, Schmidt C, Voigt N, Kamler M, et al. Phosphodiesterase 8 governs cAMP/PKA-dependent reduction of L-type calcium current in human atrial fibrillation: a novel arrhythmogenic mechanism.Eur Heart J. 2023; 44:2483–2494. doi: 10.1093/eurheartj/ehad086CrossrefMedlineGoogle Scholar13. Perera RK, Sprenger JU, Steinbrecher JH, Hubscher D, Lehnart SE, Abesser M, Schuh K, El-Armouche A, Nikolaev VO. Microdomain switch of cGMP-regulated phosphodiesterases leads to ANP-induced augmentation of beta-adrenoceptor-stimulated contractility in early cardiac hypertrophy.Circ Res. 2015; 116:1304–1311. doi: 10.1161/CIRCRESAHA.116.306082LinkGoogle Scholar14. Sumandea CA, Garcia-Cazarin ML, Bozio CH, Sievert GA, Balke CW, Sumandea MP. Cardiac troponin T, a sarcomeric AKAP, tethers protein kinase A at the myofilaments.J Biol Chem. 2011; 286:530–541. doi: 10.1074/jbc.M110.148684CrossrefMedlineGoogle Scholar eLetters(0)eLetters should relate to an article recently published in the journal and are not a forum for providing unpublished data. Comments are reviewed for appropriate use of tone and language. Comments are not peer-reviewed. Acceptable comments are posted to the journal website only. Comments are not published in an issue and are not indexed in PubMed. Comments should be no longer than 500 words and will only be posted online. References are limited to 10. Authors of the article cited in the comment will be invited to reply, as appropriate.Comments and feedback on AHA/ASA Scientific Statements and Guidelines should be directed to the AHA/ASA Manuscript Oversight Committee via its Correspondence page.Sign In to Submit a Response to This Article Previous Back to top Next FiguresReferencesRelatedDetailsRelated articlesAKAP12 Upregulation Associates With PDE8A to Accelerate Cardiac DysfunctionHanan Qasim, et al. Circulation Research. 2024;134:1006-1022 April 12, 2024Vol 134, Issue 8 Advertisement Article InformationMetrics © 2024 American Heart Association, Inc.https://doi.org/10.1161/CIRCRESAHA.124.324475PMID: 38603476 Originally publishedApril 11, 2024 KeywordsEditorialshypertrophynucleotides, cyclicphosphorylationreceptors, adrenergic, beta3',5'-cyclic-AMP phosphodiesterasesPDF download Advertisement
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